Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The autoantibodies found in human and murine systemic lupus erythematosus (SLE) are generally directed against cells or components of cells such as nuclear antigens. This predilection may be due to the unusual immunogenicity of certain autoantigens, or to unusual patterns of antibody crossreactivity. Alternatively, the observed spectrum of reactivities may reflect the in vivo absorption of those autoantibodies directed against soluble antigens. To test whether hitherto undetected autoantibodies against serum proteins might exist in murine SLE, we developed assays that were independent of the possibility of absorption of autoantibodies by serum autoantigens; large numbers of plaque-forming cells (PFC) directed against mouse albumin and mouse transferrin were easily detected in the spleens of MRL/Mp-lpr/lpr, BXSB, and NZB mice. The secreted antibodies were relatively specific for the mouse proteins, since only limited cross-reactivity was seen with albumin and transferrins of other species in inhibition experiments. The production of these hidden antibodies could not be the result of diffuse polyclonal B cell activation, since the PFC to mouse transferrins and albumin were not always accompanied by comparable numbers of PFC against related albumins and transferrins. The results indicate that autoantibody production in murine lupus is a generalized phenomenon, not limited to the production of autoantibodies to nuclear or other cell-bound antibodies. However, the relative specificity of the autoantibodies for self-antigens indicates that diffuse polyclonal B cell activation cannot be the mechanism responsible, and argues that a selective mechanism, probably driven by antigen, accounts for production of autoantibodies in SLE.
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PMID:Hidden autoantibodies against common serum proteins in murine systemic lupus erythematosus. Detection by in vitro plaque-forming cell assay. 404 Jan 53

New Zealand Black (NZB) mice develop after 16 weeks of age an autoimmune and lymphoproliferative disease which is a model for systemic lupus erythematosus and lymphoid malignancy in humans. At this age, the mice manifest a progressive decline in T lymphocyte (thymus-derived lymphocyte) functions and serum thymosin levels. Thymocytes from 8-week old NZB mice exhibit an abnormal DNA synthetic response when transplanted into lethally irradiated C57B1/6 recipients. DNA synthesis (measured as the incorporation of radioactively labeled 5-iodo-2'-deoxyuridine) is delayed in onset and still increasing 6 days after cell transfer. By contrast, 2-week old NZB thymocytes show a normal response which is rapid in onset and completed by day 6.NZB mice were injected with thymosin fraction 5 or with bovine serum albumin starting at 2 weeks of age. Thymocytes from 8-week old thymosin-treated mice showed a normal DNA synthetic response, whereas the albumin-treated controls showed the abnormal response expected at this age. The ability of thymosin to correct the DNA synthetic response was related to dose and duration of treatment. These results suggest that thymosin can induce a more normal state of thymocyte differentiation in NZB mice. If abnormal thymocyte differentiation is related to the subsequent emergence of autoimmunity and lymphoid malignancy, then continuous treatment with thymosin may have therapeutic potential. These experiments suggest that an endocrine disturbance may contribute to autoimmune and lymphoproliferative disease in NZB mice and possibly in humans.
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PMID:Thymosin corrects the abnormal DNA synthetic response of NZB mouse thymocytes. 454 60

The daily urinary albumin and beta 2-microglobulin excretion rates were measured with sensitive radioimmunoassays in 14 patients with systemic lupus erythematosus (SLE). The duration of SLE ranged from 0.5 to 18 years, mean 10 years. The mean age was 37 years. All patients except 5 received prednisone, 5-20 mg/day. None of the patients had proteinuria as judged by the "Albustix" test, and all had normal serum creatinine. The daily urinary albumin and beta 2-microglobulin excretion rates were nearly the same as those previously found by us in 27 adult control subjects with a mean age of 44 years. Our study shows that SLE patients without clinical proteinuria have a completely normal renal glomerular and tubular protein handling, irrespective of the duration of the disease.
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PMID:Urinary albumin and beta 2-microglobulin excretion rates in patients with systemic lupus erythematosus. 615 68

A solid support radioimmunoassay has been developed to detect immunoglobulin specific circulating antibodies to polyuridylic acid (Pol U), single-stranded RNA (ss RNA), and single-stranded DNA (ss DNA) in scleroderma and other connective tissue diseases. The assay system uses flex-vinyl microtiter plates on which bovine methyl albumin, the respective polynucleotide, a 1:80 dilution of patient serum, and tritiated high affinity anti-IgG, -IgA, or -IgM are layered. The individual wells containing the sandwich assay are then counted for the presence of labeled immunoglobulins and the results are reported in microgram/ml. Of the 30 scleroderma patients tested, only patients with diffuse systemic scleroderma had antibody levels reactive to Poly U > 4.0 microgram/ml and to ss RNA < 3.0 microgram/ml. Patients with linear scleroderma or morphea had antibody levels to Poly U < 3.0 microgram/ml and very little antibody to ss DNA or ss RNA in their sera. Partial cross reactivity to Poly U was found only in SLE patients with high levels of Ab to ss DNA. Insignificant levels of Poly U antibody were found in patients with other connective tissue diseases and in normal controls. High levels of serum antibody in patients which reacted with Poly U suggest active diffuse systemic scleroderma.
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PMID:Elevated levels of antibodies to polyuridylic acid detected and quantitated in systemic scleroderma patients by solid phase radioimmunoassay. 615 54

Changes in the permeability of the blood-brain barrier (BBB) and blood-cerebrospinal fluid (blood-CSF) barrier in rabbits were assessed by using a sensitive double isotope technique at different times after the induction of acute immune complex disease (AICD). Induction of AICD was done with a single large dose of bovine serum albumin, whereas controls received only saline. Animals were sacrificed 6, 9, 12, 15, and 18 days after induction. Extravasation of protein was measured by injecting rabbits i.v. with 131I-rabbit serum albumin (RSA) 24 hr before sacrifice. In order to correct for intravascular blood volume, 125I-RSA was injected 5 min before sacrifice. Extravascular blood equivalents (EVBE), a measure of barrier permeability, were elevated in the CSF of rabbits sacrificed on days 12 and 15. None of the brain regions from any of the animal groups showed any changes or significant differences from controls in EVBE values on these days. These results indicate that there was an increase in the permeability of the blood-CSF barrier to radiolabeled albumin but not in the BBB proper during the time that CSF IgG levels were elevated in AICD. The potential significance of these findings for the mechanisms mediating central nervous system involvement in systemic lupus erythematosus is discussed.
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PMID:Permeability of the blood cerebrospinal fluid barrier during acute immune complex disease. 622 64

In a 44 years old woman, a flare up of polyarthritis becoming positive for sero-reaction at the time of hospitalization, is referred to an earlier unknown SLE. The bilateral optic neuritis which began 15 years earlier, while she was pregnant, simultaneously with a bilateral carpal tunnel syndrome is retrospectively related to the SLE. Such an optic neuritis is rare, its clinical features are specified among the neuro-ophthalmological complications in SLE. Very often optic neuritis is associated with myelopathy. Hypercytosis with moderate elevation of albumin C.S.F., a high level of cyclic GMP, and a low concentration of IgG in C.S.F., are found in central neurological complications in SLE. Other biological alterations are described but both their signification and their interest, as well for diagnostic as for therapeutic supervision, are unknown. Neuropathological findings show either vasculitis or demyelinizing lesions. This case shows the therapeutic problems of such medical situations.
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PMID:[The neuro-ophthalmological complications in SLE (author's transl)]. 626 4

Thirty-nine patients with systemic lupus erythematosus (SLE) and diffuse proliferative glomerulonephritis have been enrolled in a multi-centre randomised controlled prospective study of chronic 4L plasma exchange therapy performed every three to four weeks. In the patients randomised to the pheresis (P) group and who received either albumin or plasma as replacement, there was a difference of 33 per cent better renal function at this time in the study. This difference did not achieve a significance with a p value of less than 0.05. However, the 30 patients randomised into the P group to receive albumin replacement did demonstrate a 50 per cent difference from the C group which was significant at a p value of less than 0.045. This also correlated with a statistically significant reduction in immune complex titres in the P versus the C groups. Chronic 4L plasma exchange with albumin replacement may be a useful therapeutic adjunct in patients with SLE and diffuse proliferative glomerulonephritis.
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PMID:Chronic plasma exchange in systemic lupus erythematosus nephritis. 636 59

We describe a technique for estimating the mass of anti-DNA antibodies by immunonephelometry of serum immunoglobulins (IgG, IgA, IgM) before and after adsorption onto DNA bound to agarose-polylysine columns. Sixteen patients with systemic lupus erythematosus and 16 age- and sex-matched controls were studied. Precision was determined for high-value (in 10 patients) and low-value (in nine controls) ranges for each of the immunoglobulins. Within-run CVs ranged from 3.0% (IgG, controls) to 11.8% (IgA, patients); between-run CVs ranged from 15.5% (IgG, patients) to 25.2% (IgM, patients). We found anti-DNA antibody concentrations (mean +/- SD) in systemic lupus erythematosus of 1.981 +/- 1.015 g/L for IgG (controls: 0.243 +/- 0.231, p less than 0.001), 0.257 +/- 0.215 g/L for IgA (controls: 0.038 +/- 0.035, p less than 0.001), and 0.282 +/- 0.234 g/L for IgM (controls: 0.191 +/- 0.165, p greater than 0.05). Sensitivity and linearity are such that fivefold dilutions of patients' serum with either a buffered albumin solution or control serum yielded values close to the expected values for IgG. Similarly diluted sera gave inordinately high values in the radiometric binding assay. Neither parametric (linear regression) nor nonparametric correlation methods (Spearman's rank and Kendall's tau) show a significant correlation between patients' data obtained by the present technique and that by a radiometric binding assay (p greater than 0.05), although combined data from patients and controls demonstrate a significant nonparametric correlation (p less than 0.005 for Spearman's and p less than 0.02 for Kendall's).
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PMID:Differential immunoadsorption coupled with rate nephelometry for estimation of DNA-binding immunoglobulins. 637 98

A new biocompatible collagen membrane, chemically activated in order to bind several antigens such as albumin or DNA, was successfully used to perform extracorporeal immunoadsorptions (IA) in vivo. First, immunoadsorbent devices composed of albumin-coated membranes, in a multilayer arrangement, were able to remove a large amount of anti-albumin antibodies from dogs actively immunized against heterologous albumin, during a single hemoperfusion. Second, DNA-coated membranes, in the same disposition, were used in 5 SLE-patients for serial plasma perfusions, which resulted in a significant decrease of anti-DNA antibodies (DNA-Ab) and immune complexes in serum. As previously observed in dogs, IA were sometimes followed by a rebound of DNA-Ab levels, which occurred either between successive IA (fast rebound) or 2 weeks after the series of IA, only in patients receiving the lowest steroid dosages. The main factors involved in such a rebound are probably a reequilibration of the antibody pool between the intra- and extravascular spaces, for the "fast" component of this rebound, and a de novo antibody synthesis induced by antibody removal only. Indeed, the hypothesis of a direct stimulation by either antigen release or contact between lymphocytes and antigen linked on the membrane, were ruled out by the results of in vitro studies and of plasma perfusion alone. These results support the usefulness of antigen-coated collagen membranes for in vivo IA, which represent a new approach to the treatment of autoantibody mediated diseases and to the investigation of the factors governing antibody synthesis.
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PMID:Specific adsorption of circulating antibodies by extracorporeal plasma perfusions over antigen coated collagen flat-membranes: applications to systemic lupus erythematosus. 639 94

Plasma protein loss via gastrointestinal tract was determined in 24 patients with clinical and laboratory data for manifested nephrosis syndrome, 21 of them being with various histological forms of chronic glomerulonephritis, 2--with disseminated lupus erythematosus and 1--with renal amyloidosis. Isotope labelled chromium trichloride was intravenously applied, marking the albumin pool in a dose of 0.5 micro curie (20 KBq/kg body weight). In four patients an increased fecal radio-activity was established amounting to 1.00 to 2.63 per cent of the injected dose for 96 hours. The possible causes for that phenomenon are discussed as well as its significance in the advancement of nephrosis syndrome.
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PMID:[Plasma protein loss via the gastrointestinal tract in nephrotic syndrome patients]. 667 79


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